The Origin Of Biological Information And The Higher Taxonomic Categories

PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON
117(2):2 13-239. 2004.

The origin of biological information and the
higher taxonomic categories

Stephen C. Meyer

Palm Beach Atlantic University, 901 S. Flagler Dr., West Palm Beach, Florida 33401
e-mail: stevemeyer@discovery.org

Introduction

In a recent volume of the Vienna Series
in Theoretical Biology (2003), Gerd B.
Muller and Stuart Newman argue that what
they call the “origination of organismal
form” remains an unsolved problem. In
making this claim, Muller and Newman
(2003:3-10) distinguish two distinct issues,
namely, (1) the causes of form generation
in the individual organism during embryo-
logical development and (2) the causes re-
sponsible for the production of novel or-
ganismal forms in the first place during the
history of life. To distinguish the latter case
(phylogeny) from the former (ontogeny),
Muller and Newman use the term “origi-
nation” to designate the causal processes by
which biological form first arose during the
evolution of life. They insist that “the mo-
lecular mechanisms that bring about biolog-
ical form in modem day embryos should
not be confused” with the causes respon-
sible for the origin (or “origination”) of
novel biological forms during the history of
life (p. 3). They further argue that we know
more about the causes of ontogenesis, due
to advances in molecular biology, molecu-
lar genetics and developmental biology,
than we do about the causes of phylogen-
esis — the ultimate origination of new bio-
logical forms during the remote past.

In making this claim, Muller and New-
man are careful to affirm that evolutionary
biology has succeeded in explaining how
pre-existing forms diversify under the twin
influences of natural selection and variation
of genetic traits. Sophisticated mathemati-
cally-based models of population genetics

have proven adequate for mapping and un-
derstanding quantitative variability and
populational changes in organisms. Yet
Muller and Newman insist that population
genetics, and thus evolutionary biology, has
not identified a specifically causal expla-
nation for the origin of true morphological
novelty during the history of life. Central
to their concern is what they see as the in-
adequacy of the variation of genetic traits
as a source of new form and structure. They
note, following Darwin himself, that the
sources of new form and structure must pre-
cede the action of natural selection (2003:
3) — that selection must act on what already
exists. Yet, in their view, the “genocentric-
ity” and “incrementalism” of the neo-Dar-
winian mechanism has meant that an ade-
quate source of new form and structure has
yet to be identified by theoretical biologists.
Instead, Muller and Newman see the need
to identify epigenetic sources of morpho-
logical innovation during the evolution of
life. In the meantime, however, they insist
neo-Darwinism lacks any “theory of the
generative” (p. 7).

As it happens, Muller and Newman are
not alone in this judgment. In the last de-
cade or so a host of scientific essays and
books have questioned the efficacy of se-
lection and mutation as a mechanism for
generating morphological novelty, as even
a brief literature survey will establish.
Thomson (1992:107) expressed doubt that
large-scale morphological changes could
accumulate via minor phenotypic changes
at the population genetic level. Miklos
(1993:29) argued that neo-Darwinism fails
to provide a mechanism that can produce

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large-scale innovations in form and com-
plexity. Gilbert et al. (1996) attempted to
develop a new theory of evolutionary
mechanisms to supplement classical neo-
Darwinism, which, they argued, could not
adequately explain macroevolution. As they
put it in a memorable summary of the sit-
uation: “starting in the 1970s, many biol-
ogists began questioning its [neo-Darwin-
ism’s] adequacy in explaining evolution.
Genetics might be adequate for explaining
microevolution, but microevolutionary
changes in gene frequency were not seen as
able to turn a reptile into a mammal or to
convert a fish into an amphibian. Microevo-
lution looks at adaptations that concern the
survival of the fittest, not the arrival of the
fittest. As Goodwin (1995) points out, ‘the
origin of species — Darwin’s problem — re-
mains unsolved’ ” (p. 361). Though Gilbert
et al. (1996) attempted to solve the problem
of the origin of form by proposing a greater
role for developmental genetics within an
otherwise neo-Darwinian framework, 1 nu-
merous recent authors have continued to
raise questions about the adequacy of that
framework itself or about the problem of
the origination of form generally (Webster
& Goodwin 1996; Shubin & Marshall
2000; Erwin 2000; Conway Morris 2000,
2003b; Carrol 2000; Wagner 2001; Becker
& Lonnig 2001; Stadler et al. 2001; Lonnig
& Saedler 2002; Wagner & Stadler 2003;
Valentine 2004:189-194).

What lies behind this skepticism? Is it
warranted? Is a new and specifically causal
theory needed to explain the origination of
biological form?

This review will address these questions.
It will do so by analyzing the problem of
the origination of organismal form (and the

1 Specifically, Gilbert et al. (1996) argued that
changes in morphogenetic fields might produce large-
scale changes in the developmental programs and, ul-
timately, body plans of organisms. Yet they offered no
evidence that such fields — if indeed they exist — can
be altered to produce advantageous variations in body
plan, though this is a necessary condition of any suc-
cessful causal theory of macroevolution.

corresponding emergence of higher taxa)
from a particular theoretical standpoint.
Specifically, it will treat the problem of the
origination of the higher taxonomic groups
as a manifestation of a deeper problem,
namely, the problem of the origin of the
information (whether genetic or epigenetic)
that, as it will be argued, is necessary to
generate morphological novelty.

In order to perform this analysis, and to
make it relevant and tractable to systema-
tists and paleontologists, this paper will ex-
amine a paradigmatic example of the origin
of biological form and information during
the history of life: the Cambrian explosion.
During the Cambrian, many novel animal
forms and body plans (representing new
phyla, sub-phyla and classes) arose in a
geologically brief period of time. The fol-
lowing information-based analysis of the
Cambrian explosion will support the claim
of recent authors such as Muller and New-
man that the mechanism of selection and
genetic mutation does not constitute an ad-
equate causal explanation of the origination
of biological form in the higher taxonomic
groups. It will also suggest the need to ex-
plore other possible causal factors for the
origin of form and information during the
evolution of life and will examine some
other possibilities that have been proposed.

The Cambrian Explosion

The “Cambrian explosion” refers to the
geologically sudden appearance of many
new animal body plans about 530 million
years ago. At this time, at least nineteen,
and perhaps as many as thirty-five phyla of
forty total (Meyer et al. 2003), made their
first appearance on Earth within a narrow
five- to ten-million-year window of geolog-
ic time (Bowring et al. 1993, 1998a:l,
1998b:40; Kerr 1993; Monastersky 1993;
Aris-Brosou & Yang 2003). Many new sub-
phyla, between 32 and 48 of 56 total (Mey-
er et al. 2003), and classes of animals also
arose at this time with representatives of
these new higher taxa manifesting signifi-

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215

cant morphological innovations. The Cam-
brian explosion thus marked a major epi-
sode of morphogenesis in which many new
and disparate organismal forms arose in a
geologically brief period of time.

To say that the fauna of the Cambrian
period appeared in a geologically sudden
manner also implies the absence of clear
transitional intermediate forms connecting
Cambrian animals with simpler pre-Cam-
brian forms. And, indeed, in almost all cas-
es, the Cambrian animals have no clear
morphological antecedents in earlier Ven-
dian or Precambrian fauna (Miklos 1993,
Erwin et al. 1997:132, Steiner & Reitner
2001, Conway Morris 2003b:510, Valentine
et al. 2003:519-520). Further, several re-
cent discoveries and analyses suggest that
these morphological gaps may not be mere-
ly an artifact of incomplete sampling of the
fossil record (Foote 1997, Foote et al. 1999,
Benton & Ayala 2003, Meyer et al. 2003),
suggesting that the fossil record is at least
approximately reliable (Conway Morris
2003b:505).

As a result, debate now exists about the
extent to which this pattern of evidence
comports with a strictly monophyletic view
of evolution (Conway Morris 1998a, 2003a,
2003b:510; Willmer 1990, 2003). Further,
among those who accept a monophyletic
view of the history of life, debate exists
about whether to privilege fossil or molec-
ular data and analyses. Those who think the
fossil data provide a more reliable picture of
the origin of the Metazoan tend to think
these animals arose relatively quickly — that
the Cambrian explosion had a “short fuse.”
(Conway Morris 2003b:505-506, Valentine
& Jablonski 2003). Some (Wray et al. 1996),
but not all (Ayala et al. 1998), who think
that molecular phylogenies establish reliable
divergence times from pre-Cambrian ances-
tors think that the Cambrian animals evolved
over a very long period of time — that the
Cambrian explosion had a “long fuse.” This
review will not address these questions of
historical pattern. Instead, it will analyze
whether the neo-Darwinian process of mu-

tation and selection, or other processes of
evolutionary change, can generate the form
and information necessary to produce the
animals that arise in the Cambrian. This
analysis will, for the most part, 2 therefore,
not depend upon assumptions of either a
long or short fuse for the Cambrian explo-
sion, or upon a monophyletic or polyphyletic
view of the early history of life.

Defining Biological Form and Information

Form, like life itself, is easy to recognize
but often hard to define precisely. Yet, a rea-
sonable working definition of form will suf-
fice for our present purposes. Form can be
defined as the four-dimensional topological
relations of anatomical parts. This means that
one can understand form as a unified arrange-
ment of body parts or material components
in a distinct shape or pattern (topology) — one
that exists in three spatial dimensions and
which arises in time during ontogeny.

Insofar as any particular biological form
constitutes something like a distinct ar-
rangement of constituent body parts, form
can be seen as arising from constraints that
limit the possible arrangements of matter.
Specifically, organismal form arises (both
in phylogeny and ontogeny) as possible ar-
rangements of material parts are con-
strained to establish a specific or particular
arrangement with an identifiable three di-
mensional topography — one that we would
recognize as a particular protein, cell type,
organ, body plan or organism. A particular

2 If one takes the fossil record at face value and
assumes that the Cambrian explosion took place within
a relatively narrow 5-1 0 million year window, explain-
ing the origin of the information necessary to produce
new proteins, for example, becomes more acute in part
because mutation rates would not have been sufficient
to generate the number of changes in the genome nec-
essary to build the new proteins for more complex
Cambrian animals (Ohno 1996:8475-8478). This re-
view will argue that, even if one allows several hun-
dred million years for the origin of the metazoan, sig-
nificant probabilistic and other difficulties remain with
the neo-Darwinian explanation of the origin of form
and information.

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“form,” therefore, represents a highly spe-
cific and constrained arrangement of mate-
rial components (among a much larger set
of possible arrangements).

Understanding form in this way suggests
a connection to the notion of information in
its most theoretically general sense. When
Shannon (1948) first developed a mathe-
matical theory of information he equated
the amount of information transmitted with
the amount of uncertainty reduced or elim-
inated in a series of symbols or characters.
Information, in Shannon’s theory, is thus
imparted as some options are excluded and
others are actualized. The greater the num-
ber of options excluded, the greater the
amount of information conveyed. Further,
constraining a set of possible material ar-
rangements by whatever process or means
involves excluding some options and actu-
alizing others. Thus, to constrain a set of
possible material states is to generate infor-
mation in Shannon’s sense. It follows that
the constraints that produce biological form
also impart in/brmation. Or conversely, one
might say that producing organismal form
by definition requires the generation of in-
formation.

In classical Shannon information theory,
the amount of information in a system is
also inversely related to the probability of
the arrangement of constituents in a system
or the characters along a communication
channel (Shannon 1948). The more improb-
able (or complex) the arrangement, the
more Shannon information, or information-
carrying capacity, a string or system pos-
sesses.

Since the 1960s, mathematical biologists
have realized that Shannon’s theory could
be applied to the analysis of DNA and pro-
teins to measure the information-carrying
capacity of these macromolecules. Since
DNA contains the assembly instructions for
building proteins, the information-process-
ing system in the cell represents a kind of
communication channel (Yockey 1992:
110). Further, DNA conveys information
via specifically arranged sequences of nu-

cleotide bases. Since each of the four bases
has a roughly equal chance of occurring at
each site along the spine of the DNA mol-
ecule, biologists can calculate the probabil-
ity, and thus the information-carrying ca-
pacity, of any particular sequence n bases
long.

The ease with which information theory
applies to molecular biology has created
confusion about the type of information that
DNA and proteins possess. Sequences of
nucleotide bases in DNA, or amino acids in
a protein, are highly improbable and thus
have large information-carrying capacities.
But, like meaningful sentences or lines of
computer code, genes and proteins are also
specified with respect to function. Just as
the meaning of a sentence depends upon the
specific arrangement of the letters in a sen-
tence, so too does the function of a gene
sequence depend upon the specific arrange-
ment of the nucleotide bases in a gene.
Thus, molecular biologists beginning with
Crick equated information not only with
complexity but also with “specificity,”
where “specificity” or “specified” has
meant “necessary to function” (Crick
1958:144, 153; Sarkar, 1996:191). 3 Molec-
ular biologists such as Monod and Crick
understood biological information — the in-
formation stored in DNA and proteins — as
something more than mere complexity (or
improbability). Their notion of information
associated both biochemical contingency
and combinatorial complexity with DNA
sequences (allowing DNA’s carrying capac-
ity to be calculated), but it also affirmed
that sequences of nucleotides and amino ac-
ids in functioning macromolecules pos-
sessed a high degree of specificity relative
to the maintenance of cellular function.

The ease with which information theory
applies to molecular biology has also cre-
ated confusion about the location of infor-

3 As Crick put it, “information means here the pre-
cise determination of sequence, either of bases in the
nucleic acid or on amino acid residues in the protein”
(Crick 1958:144, 153).

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217

mation in organisms. Perhaps because the
information carrying capacity of the gene
could be so easily measured, it has been
easy to treat DNA, RNA and proteins as the
sole repositories of biological information.
Neo-Darwinists in particular have assumed
that the origination of biological form could
be explained by recourse to processes of ge-
netic variation and mutation alone (Levin-
ton 1988:485). Yet if one understands or-
ganismal form as resulting from constraints
on the possible arrangements of matter at
many levels in the biological hierarchy —
from genes and proteins to cell types and
tissues to organs and body plans — then
clearly biological organisms exhibit many
levels of information-rich structure.

Thus, we can pose a question, not only
about the origin of genetic information, but
also about the origin of the information nec-
essary to generate form and structure at lev-
els higher than that present in individual
proteins. We must also ask about the origin
of the “specified complexity,” as opposed
to mere complexity, that characterizes the
new genes, proteins, cell types and body
plans that arose in the Cambrian explosion.
Dembski (2002) has used the term “com-
plex specified information” (CSI) as a syn-
onym for “specified complexity” to help
distinguish functional biological informa-
tion from mere Shannon information — that
is, specified complexity from mere com-
plexity. This review will use this term as
well.

The Cambrian Information Explosion

The Cambrian explosion represents a re-
markable jump in the specified complexity
or “complex specified information” (CSI)
of the biological world. For over three bil-
lion years, the biological realm included lit-
tle more than bacteria and algae (Brocks et
al. 1999). Then, beginning about 570-565
million years ago (mya), the first complex
multicellular organisms appeared in the
rock strata, including sponges, cnidarians,
and the peculiar Ediacaran biota (Grotzin-

ger et al. 1995). Forty million years later,
the Cambrian explosion occurred (Bowring
et al. 1993). The emergence of the Edi-
acaran biota (570 mya), and then to a much
greater extent the Cambrian explosion (530
mya), represented steep climbs up the bio-
logical complexity gradient.

One way to estimate the amount of new
CSI that appeared with the Cambrian ani-
mals is to count the number of new cell
types that emerged with them (Valentine
1995:91-93). Studies of modem animals
suggest that the sponges that appeared in
the late Precambrian, for example, would
have required five cell types, whereas the
more complex animals that appeared in the
Cambrian (e.g., arthropods) would have re-
quired fifty or more cell types. Functionally
more complex animals require more cell
types to perform their more diverse func-
tions. New cell types require many new and
specialized proteins. New proteins, in turn,
require new genetic information. Thus an
increase in the number of cell types implies
(at a minimum) a considerable increase in
the amount of specified genetic informa-
tion. Molecular biologists have recently es-
timated that a minimally complex single-
celled organism would require between 3 1 8
and 562 kilobase pairs of DNA to produce
the proteins necessary to maintain life
(Koonin 2000). More complex single cells
might require upward of a million base
pairs. Yet to build the proteins necessary to
sustain a complex arthropod such as a tri-
lobite would require orders of magnitude
more coding instructions. The genome size
of a modern arthropod, the fruitfly Dro-
sophila melanogaster, is approximately 1 80
million base pairs (Gerhart & Kirschner
1997:121, Adams et al. 2000). Transitions
from a single cell to colonies of cells to
complex animals represent significant (and,
in principle, measurable) increases in CSI.

Building a new animal from a single-
celled organism requires a vast amount of
new genetic information. It also requires a
way of arranging gene products — pro-
teins — into higher levels of organization.

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New proteins are required to service new
cell types. But new proteins must be orga-
nized into new systems within the cell; new
cell types must be organized into new tis-
sues, organs, and body parts. These, in turn,
must be organized to form body plans. New
animals, therefore, embody hierarchically
organized systems of lower-level parts
within a functional whole. Such hierarchi-
cal organization itself represents a type of
information, since body plans comprise
both highly improbable and functionally
specified arrangements of lower-level parts.
The specified complexity of new body
plans requires explanation in any account of
the Cambrian explosion.

Can neo-Darwinism explain the discon-
tinuous increase in CSI that appears in the
Cambrian explosion — either in the form of
new genetic information or in the form of
hierarchically organized systems of parts?
We will now examine the two parts of this
question.

Novel Genes and Proteins

Many scientists and mathematicians have
questioned the ability of mutation and se-
lection to generate information in the form
of novel genes and proteins. Such skepti-
cism often derives from consideration of
the extreme improbability (and specificity)
of functional genes and proteins.

A typical gene contains over one thousand
precisely arranged bases. For any specific ar-
rangement of four nucleotide bases of length
n, there is a corresponding number of pos-
sible arrangements of bases, 4". For any pro-
tein, there are 20" possible arrangements of
protein-forming amino acids. A gene 999
bases in length represents one of 4 999 possi-
ble nucleotide sequences; a protein of 333
amino acids is one of 20 333 possibilities.

Since the 1960s, some biologists have
thought functional proteins to be rare among
the set of possible amino acid sequences.
Some have used an analogy with human lan-
guage to illustrate why this should be the
case. Denton (1986, 309-31 1), for example.

has shown that meaningful words and sen-
tences are extremely rare among the set of
possible combinations of English letters, es-
pecially as sequence length grows. (The ra-
tio of meaningful 12-letter words to 12-letter
sequences is 1/10 14 ; the ratio of 100-letter
sentences to possible 100-letter strings is
1/1 0 100 .) Further, Denton shows that most
meaningful sentences are highly isolated
from one another in the space of possible
combinations, so that random substitutions
of letters will, after a very few changes, in-
evitably degrade meaning. Apart from a few
closely clustered sentences accessible by
random substitution, the overwhelming ma-
jority of meaningful sentences lie, probabi-
listically speaking, beyond the reach of ran-
dom search.

Denton (1986:301-324) and others have
argued that similar constraints apply to
genes and proteins. They have questioned
whether an undirected search via mutation
and selection would have a reasonable
chance of locating new islands of func-
tion — representing fundamentally new
genes or proteins — within the time avail-
able (Eden 1967, Shiitzenberger 1967,
Lpvtrup 1979). Some have also argued that
alterations in sequencing would likely result
in loss of protein function before funda-
mentally new function could arise (Eden
1967, Denton 1986). Nevertheless, neither
the extent to which genes and proteins are
sensitive to functional loss as a result of
sequence change, nor the extent to which
functional proteins are isolated within se-
quence space, has been fully known.

Recently, experiments in molecular biol-
ogy have shed light on these questions. A
variety of mutagenesis techniques have
shown that proteins (and thus the genes that
produce them) are indeed highly specified
relative to biological function (Bowie &
Sauer 1989, Reidhaar-Olson & Sauer 1990,
Taylor et al. 2001). Mutagenesis research
tests the sensitivity of proteins (and, by im-
plication, DNA) to functional loss as a result
of alterations in sequencing. Studies of pro-
teins have long shown that amino acid res-

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219

idues at many active positions cannot vary
without functional loss (Perutz & Lehmann
1968). More recent protein studies (often us-
ing mutagenesis experiments) have shown
that functional requirements place significant
constraints on sequencing even at non-active
site positions (Bowie & Sauer 1989, Reid-
haar-Olson & Sauer 1990, Chothia et al.
1998, Axe 2000, Taylor et al. 2001). In par-
ticular, Axe (2000) has shown that multiple
as opposed to single position amino acid
substitutions inevitably result in loss of pro-
tein function, even when these changes oc-
cur at sites that allow variation when altered
in isolation. Cumulatively, these constraints
imply that proteins are highly sensitive to
functional loss as a result of alterations in
sequencing, and that functional proteins rep-
resent highly isolated and improbable ar-
rangements of amino acids — arrangements
that are far more improbable, in fact, than
would be likely to arise by chance alone in
the time available (Reidhaar-Olson & Sauer
1990; Behe 1992; Kauffman 1995:44;
Dembski 1998:175-223; Axe 2000, 2004).
(See below the discussion of the neutral the-
ory of evolution for a precise quantitative
assessment.)

Of course, neo-Darwinists do not envi-
sion a completely random search through
the set of all possible nucleotide sequenc-
es — so-called “sequence space.” They en-
vision natural selection acting to preserve
small advantageous variations in genetic se-
quences and their corresponding protein
products. Dawkins (1996), for example, lik-
ens an organism to a high mountain peak.
He compares climbing the sheer precipice
up the front side of the mountain to build-
ing a new organism by chance. He ac-
knowledges that this approach up “Mount
Improbable” will not succeed. Neverthe-
less, he suggests that there is a gradual
slope up the backside of the mountain that
could be climbed in small incremental
steps. In his analogy, the backside climb up
“Mount Improbable” corresponds to the
process of natural selection acting on ran-
dom changes in the genetic text. What

chance alone cannot accomplish blindly or
in one leap, selection (acting on mutations)
can accomplish through the cumulative ef-
fect of many slight successive steps.

Yet the extreme specificity and complex-
ity of proteins presents a difficulty, not only
for the chance origin of specified biological
information (i.e., for random mutations act-
ing alone), but also for selection and muta-
tion acting in concert. Indeed, mutagenesis
experiments cast doubt on each of the two
scenarios by which neo-Darwinists envision
new information arising from the mutation/
selection mechanism (for review, see Lonnig
2001). For neo-Darwinism, new functional
genes either arise from non-coding sections
in the genome or from preexisting genes.
Both scenarios are problematic.

In the first scenario, neo-Darwinists en-
vision new genetic information arising from
those sections of the genetic text that can
presumably vary freely without conse-
quence to the organism. According to this
scenario, non-coding sections of the ge-
nome, or duplicated sections of coding re-
gions, can experience a protracted period of
“neutral evolution” (Kimura 1983) during
which alterations in nucleotide sequences
have no discernible effect on the function
of the organism. Eventually, however, a
new gene sequence will arise that can code
for a novel protein. At that point, natural
selection can favor the new gene and its
functional protein product, thus securing
the preservation and heritability of both.

This scenario has the advantage of allow-
ing the genome to vary through many gen-
erations, as mutations “search” the space
of possible base sequences. The scenario
has an overriding problem, however: the
size of the combinatorial space (i.e., the
number of possible amino acid sequences)
and the extreme rarity and isolation of the
functional sequences within that space of
possibilities. Since natural selection can do
nothing to help generate new functional se-
quences, but rather can only preserve such
sequences once they have arisen, chance
alone — random variation — must do the

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work of information generation — that is, of
finding the exceedingly rare functional se-
quences within the set of combinatorial
possibilities. Yet the probability of random-
ly assembling (or “finding,” in the previous
sense) a functional sequence is extremely
small.

Cassette mutagenesis experiments per-
formed during the early 1990s suggest that
the probability of attaining (at random) the
correct sequencing for a short protein 100
amino acids long is about 1 in 10 65 (Reid-
haar-Olson & Sauer 1990, Behe 1992:65-
69). This result agreed closely with earlier
calculations that Yockey (1978) had per-
formed based upon the known sequence
variability of cytochrome c in different spe-
cies and other theoretical considerations.
More recent mutagenesis research has pro-
vided additional support for the conclusion
that functional proteins are exceedingly rare
among possible amino acid sequences (Axe
2000, 2004). Axe (2004) has performed site
directed mutagenesis experiments on a 150-
residue protein-folding domain within a (3-
lactamase enzyme. His experimental meth-
od improves upon earlier mutagenesis tech-
niques and corrects for several sources of
possible estimation error inherent in them.
On the basis of these experiments, Axe has
estimated the ratio of (a) proteins of typical
size (150 residues) that perform a specified
function via any folded structure to (b) the
whole set of possible amino acids sequenc-
es of that size. Based on his experiments.
Axe has estimated this ratio to be 1 to 10 77 .
Thus, the probability of finding a functional
protein among the possible amino acid se-
quences corresponding to a 150-residue
protein is similarly 1 in 10 77 .

Other considerations imply additional
improbabilities. First, new Cambrian ani-
mals would require proteins much longer
than 100 residues to perform many neces-
sary specialized functions. Ohno (1996) has
noted that Cambrian animals would have
required complex proteins such as lysyl ox-
idase in order to support their stout body
structures. Lysyl oxidase molecules in ex-

tant organisms comprise over 400 amino
acids. These molecules are both highly
complex (non-repetitive) and functionally
specified. Reasonable extrapolation from
mutagenesis experiments done on shorter
protein molecules suggests that the proba-
bility of producing functionally sequenced
proteins of this length at random is so small
as to make appeals to chance absurd, even
granting the duration of the entire universe.
(See Dembski 1998:175-223 for a rigorous
calculation of this “Universal Probability
Bound”; See also Axe 2004.) Yet, second,
fossil data (Bowring et al. 1993, 1998a: 1,
1998b:40; Kerr 1993; Monastersky 1993),
and even molecular analyses supporting
deep divergence (Wray et al. 1 996), suggest
that the duration of the Cambrian explosion
(between 5-10 X 10 6 and, at most, 7 X 10 7
years) is far smaller than that of the entire
universe (1.3—2 X 10 10 years). Third, DNA
mutation rates are far too low to generate
the novel genes and proteins necessary to
building the Cambrian animals, given the
most probable duration of the explosion as
determined by fossil studies (Conway Mor-
ris 1998b). As Ohno (1996:8475) notes,
even a mutation rate of 10 -9 per base pair
per year results in only a 1 % change in the
sequence of a given section of DNA in 10
million years. Thus, he argues that muta-
tional divergence of pre-existing genes can-
not explain the origin of the Cambrian
forms in that time. 4

4 To solve this problem Ohno himself proposes the
existence of a hypothetical ancestral form that pos-
sessed virtually all the genetic information necessary
to produce the new body plans of the Cambrian ani-
mals. He asserts that this ancestor and its “panani-
malian genome” might have arisen several hundred
million years before the Cambrian explosion. On this
view, each of the different Cambrian animals would
have possessed virtually identical genomes, albeit with
considerable latent and unexpressed capacity in the
case of each individual form (Ohno 1996:8475-8478).
While this proposal might help explain the origin of
the Cambrian animal forms by reference to pre-exist-
ing genetic information, it does not solve, but instead
merely displaces, the problem of the origin of the ge-
netic information necessary to produce these new
forms.

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221

The selection/mutation mechanism faces
another probabilistic obstacle. The animals
that arise in the Cambrian exhibit struc-
tures that would have required many new
types of cells, each of which would have
required many novel proteins to perform
their specialized functions. Further, new
cell types require systems of proteins that
must, as a condition of functioning, act in
close coordination with one another. The
unit of selection in such systems ascends
to the system as a whole. Natural selection
selects for functional advantage. But new
cell types require whole systems of pro-
teins to perform their distinctive functions.
In such cases, natural selection cannot con-
tribute to the process of information gen-
eration until after the information neces-
sary to build the requisite system of pro-
teins has arisen. Thus random variations
must, again, do the work of information
generation — and now not simply for one
protein, but for many proteins arising at
nearly the same time. Yet the odds of this
occurring by chance alone are, of course,
far smaller than the odds of the chance or-
igin of a single gene or protein — so small
in fact as to render the chance origin of the
genetic information necessary to build a
new cell type (a necessary but not suffi-
cient condition of building a new body
plan) problematic given even the most op-
timistic estimates for the duration of the
Cambrian explosion.

Dawkins (1986:139) has noted that sci-
entific theories can rely on only so much
“luck” before they cease to be credible.
The neutral theory of evolution, which, by
its own logic, prevents natural selection
from playing a role in generating genetic
information until after the fact, relies on
entirely too much luck. The sensitivity of
proteins to functional loss, the need for
long proteins to build new cell types and
animals, the need for whole new systems
of proteins to service new cell types, the
probable brevity of the Cambrian explo-
sion relative to mutation rates — all suggest
the immense improbability (and implausi-

bility) of any scenario for the origination
of Cambrian genetic information that relies
upon random variation alone unassisted by
natural selection.

Yet the neutral theory requires novel
genes and proteins to arise — essentially —
by random mutation alone. Adaptive advan-
tage accrues after the generation of new
functional genes and proteins. Thus, natural
selection cannot play a role until new in-
formation-bearing molecules have indepen-
dently arisen. Thus neutral theorists envi-
sion the need to scale the steep face of a
Dawkins-style precipice of which there is
no gradually sloping backside — a situation
that, by Dawkins’ own logic, is probabilis-
tically untenable.

In the second scenario, neo-Darwinists
envision novel genes and proteins arising
by numerous successive mutations in the
preexisting genetic text that codes for pro-
teins. To adapt Dawkins’s metaphor, this
scenario envisions gradually climbing
down one functional peak and then as-
cending another. Yet mutagenesis experi-
ments again suggest a difficulty. Recent
experiments show that, even when explor-
ing a region of sequence space populated
by proteins of a single fold and function,
most multiple-position changes quickly
lead to loss of function (Axe 2000). Yet to
turn one protein into another with a com-
pletely novel structure and function re-
quires specified changes at many sites. In-
deed, the number of changes necessary to
produce a new protein greatly exceeds the
number of changes that will typically pro-
duce functional losses. Given this, the
probability of escaping total functional
loss during a random search for the chang-
es needed to produce a new function is ex-
tremely small — and this probability dimin-
ishes exponentially with each additional
requisite change (Axe 2000). Thus, Axe’s
results imply that, in all probability, ran-
dom searches for novel proteins (through
sequence space) will result in functional
loss long before any novel functional pro-
tein will emerge.

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Blanco et al. have come to a similar con-
clusion. Using directed mutagenesis, they
have determined that residues in both the
hydrophobic core and on the surface of the
protein play essential roles in determining
protein structure. By sampling intermediate
sequences between two naturally occurring
sequences that adopt different folds, they
found that the intermediate sequences “lack
a well defined three-dimensional structure.”
Thus, they conclude that it is unlikely that
a new protein fold would evolve from a
pre-existing fold via a series of folded in-
termediates sequences (Blanco et al. 1999:
741).

Thus, although this second neo-Darwin-
ian scenario has the advantage of starting
with functional genes and proteins, it also
has a lethal disadvantage: any process of
random mutation or rearrangement in the
genome would in all probability generate
nonfunctional intermediate sequences be-
fore fundamentally new functional genes or
proteins would arise. Clearly, nonfunctional
intermediate sequences confer no survival
advantage on their host organisms. Natural
selection favors only functional advantage.
It cannot select or favor nucleotide se-
quences or polypeptide chains that do not
yet perform biological functions, and still
less will it favor sequences that efface or
destroy preexisting function.

Evolving genes and proteins will range
through a series of nonfunctional interme-
diate sequences that natural selection will
not favor or preserve but will, in all prob-
ability, eliminate (Blanco et al. 1999, Axe
2000). When this happens, selection-driven
evolution will cease. At this point, neutral
evolution of the genome (unhinged from se-
lective pressure) may ensue, but, as we
have seen, such a process must overcome
immense probabilistic hurdles, even grant-
ing cosmic time.

Thus, whether one envisions the evolu-
tionary process beginning with a noncoding
region of the genome or a preexisting func-
tional gene, the functional specificity and
complexity of proteins impose very strin-

gent limitations on the efficacy of mutation
and selection. In the first case, function
must arise first, before natural selection can
act to favor a novel variation. In the second
case, function must be continuously main-
tained in order to prevent deleterious (or le-
thal) consequences to the organism and to
allow further evolution. Yet the complexity
and functional specificity of proteins im-
plies that both these conditions will be ex-
tremely difficult to meet. Therefore, the
neo-Darwinian mechanism appears to be
inadequate to generate the new information
present in the novel genes and proteins that
arise with the Cambrian animals.

Novel Body Plans

The problems with the neo-Darwinian
mechanism run deeper still. In order to ex-
plain the origin of the Cambrian animals,
one must account not only for new proteins
and cell types, but also for the origin of new
body plans. Within the past decade, devel-
opmental biology has dramatically ad-
vanced our understanding of how body
plans are built during ontogeny. In the pro-
cess, it has also uncovered a profound dif-
ficulty for neo-Darwinism.

Significant morphological change in or-
ganisms requires attention to timing. Mu-
tations in genes that are expressed late in
the development of an organism will not
affect the body plan. Mutations expressed
early in development, however, could con-
ceivably produce significant morphological
change (Arthur 1997:21). Thus, events ex-
pressed early in the development of organ-
isms have the only realistic chance of pro-
ducing large-scale macroevolutionary
change (Thomson 1992). As John and Mik-
los (1988:309) explain, macroevolutionary
change requires alterations in the very early
stages of ontogenesis.

Yet recent studies in developmental bi-
ology make clear that mutations expressed
early in development typically have dele-
terious effects (Arthur 1997:21). For ex-
ample, when early-acting body plan mol-

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223

ecules, or morphogens such as bicoid
(which helps to set up the anterior-poste-
rior head-to-tail axis in Drosophila), are
perturbed, development shuts down (Niis-
slein-Volhard & Wieschaus 1980, Lawr-
ence & Struhl 1996, Muller & Newman
2003). 5 The resulting embryos die. More-
over, there is a good reason for this. If an
engineer modifies the length of the piston
rods in an internal combustion engine
without modifying the crankshaft accord-
ingly, the engine won’t start. Similarly,
processes of development are tightly inte-
grated spatially and temporally such that
changes early in development will require
a host of other coordinated changes in sep-
arate but functionally interrelated devel-
opmental processes downstream. For this
reason, mutations will be much more likely
to be deadly if they disrupt a functionally
deeply-embedded structure such as a spinal
column than if they affect more isolated
anatomical features such as fingers (Kauff-
man 1995:200).

This problem has led to what McDonald
(1983) has called “a great Darwinian par-
adox” (p. 93). McDonald notes that genes
that are observed to vary within natural
populations do not lead to major adaptive
changes, while genes that could cause ma-
jor changes — the very stuff of macroevo-
lution — apparently do not vary. In other
words, mutations of the kind that macro-
evolution doesn’t need (namely, viable ge-
netic mutations in DNA expressed late in
development) do occur, but those that it
does need (namely, beneficial body plan
mutations expressed early in development)

5 Some have suggested that mutations in “master
regulator” Hox genes might provide the raw material
for body plan morphogenesis. Yet there are two prob-
lems with this proposal. First, Hox gene expression
begins only after the foundation of the body plan has
been established in early embryogenesis (Davidson
2001:66). Second, Hox genes are highly conserved
across many disparate phyla and so cannot account for
the morphological differences that exist between the
phyla (Valentine 2004:88).

apparently don’t occur. 6 According to Dar-
win (1859:108) natural selection cannot act
until favorable variations arise in a popu-
lation. Yet there is no evidence from de-
velopmental genetics that the kind of vari-
ations required by neo-Darwinism — name-
ly, favorable body plan mutations — ever
occur.

Developmental biology has raised anoth-
er formidable problem for the mutation/se-
lection mechanism. Embryological evi-
dence has long shown that DNA does not
wholly determine morphological form
(Goodwin 1985, Nijhout 1990, Sapp 1987,
Muller & Newman 2003), suggesting that
mutations in DNA alone cannot account for
the morphological changes required to build
a new body plan.

DNA helps directs protein synthesis. 7 It
also helps to regulate the timing and ex-
pression of the synthesis of various proteins
within cells. Yet, DNA alone does not de-
termine how individual proteins assemble
themselves into larger systems of proteins;
still less does it solely determine how cell
types, tissue types, and organs arrange
themselves into body plans (Harold 1995:

6 Notable differences in the developmental pathways
of similar organisms have been observed. For exam-
ple, congeneric species of sea urchins (from genus He-
liocidaris ) exhibit striking differences in their devel-
opmental pathways (Raff 1999:110-121). Thus, it
might be argued that such differences show that early
developmental programs can in fact be mutated to pro-
duce new forms. Nevertheless, there are two problems
with this claim. First, there is no direct evidence that
existing differences in sea urchin development arose
by mutation. Second, the observed differences in the
developmental programs of different species of sea ur-
chins do not result in new body plans, but instead in
highly conserved structures. Despite differences in de-
velopmental patterns, the endpoints are the same.
Thus, even if it can be assumed that mutations pro-
duced the differences in developmental pathways, it
must be acknowledged that such changes did not result
in novel form.

7 Of course, many post-translation processes of
modification also play a role in producing a functional
protein. Such processes make it impossible to predict
a protein’s final sequencing from its corresponding
gene sequence alone (Sarkar 1996:199-202).

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2774, Moss 2004). Instead, other factors —
such as the three-dimensional structure and
organization of the cell membrane and cy-
toskeleton and the spatial architecture of the
fertilized egg — play important roles in de-
termining body plan formation during em-
bryogenesis.

For example, the structure and location
of the cytoskeleton influence the patterning
of embryos. Arrays of microtubules help to
distribute the essential proteins used during
development to their correct locations in the
cell. Of course, microtubules themselves
are made of many protein subunits. Nev-
ertheless, like bricks that can be used to as-
semble many different structures, the tu-
bulin subunits in the cell’s microtubules are
identical to one another. Thus, neither the
tubulin subunits nor the genes that produce
them account for the different shape of mi-
crotubule arrays that distinguish different
kinds of embryos and developmental path-
ways. Instead, the structure of the micro-
tubule array itself is determined by the lo-
cation and arrangement of its subunits, not
the properties of the subunits themselves.
For this reason, it is not possible to predict
the structure of the cytoskeleton of the cell
from the characteristics of the protein con-
stituents that form that structure (Harold
2001:125).

Two analogies may help further clarify
the point. At a building site, builders will
make use of many materials: lumber, wires,
nails, drywall, piping, and windows. Yet
building materials do not determine the
floor plan of the house, or the arrangement
of houses in a neighborhood. Similarly,
electronic circuits are composed of many
components, such as resistors, capacitors,
and transistors. But such lower-level com-
ponents do not determine their own ar-
rangement in an integrated circuit. Biolog-
ical systems also depend on hierarchical ar-
rangements of parts. Genes and proteins are
made from simple building blocks — nucle-
otide bases and amino acids — arranged in
specific ways. Cell types are made of,
among other things, systems of specialized

proteins. Organs are made of specialized ar-
rangements of cell types and tissues. And
body plans comprise specific arrangements
of specialized organs. Yet, clearly, the prop-
erties of individual proteins (or, indeed, the
lower-level parts in the hierarchy generally)
do not fully determine the organization of
the higher-level structures and organization-
al patterns (Harold 2001:125). It follows
that the genetic information that codes for
proteins does not determine these higher-
level structures either.

These considerations pose another chal-
lenge to the sufficiency of the neo-Darwin-
ian mechanism. Neo-Darwinism seeks to
explain the origin of new information,
form, and structure as a result of selection
acting on randomly arising variation at a
very low level within the biological hier-
archy, namely, within the genetic text. Yet
major morphological innovations depend
on a specificity of arrangement at a much
higher level of the organizational hierarchy,
a level that DNA alone does not determine.
Yet if DNA is not wholly responsible for
body plan morphogenesis, then DNA se-
quences can mutate indefinitely, without re-
gard to realistic probabilistic limits, and still
not produce a new body plan. Thus, the
mechanism of natural selection acting on
random mutations in DNA cannot in prin-
ciple generate novel body plans, including
those that first arose in the Cambrian ex-
plosion.

Of course, it could be argued that, while
many single proteins do not by themselves
determine cellular structures and/or body
plans, proteins acting in concert with other
proteins or suites of proteins could deter-
mine such higher-level form. For example,
it might be pointed out that the tubulin sub-
units (cited above) are assembled by other
helper proteins — gene products — called Mi-
crotubule Associated Proteins (MAPS).
This might seem to suggest that genes and
gene products alone do suffice to determine
the development of the three-dimensional
structure of the cytoskeleton.

Yet, MAPS, and indeed many other nec-

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225

essary proteins, are only part of the story.
The location of specified target sites on the
interior of the cell membrane also helps to
determine the shape of the cytoskeleton.
Similarly, so does the position and structure
of the centrosome which nucleates the mi-
crotubules that form the cytoskeleton.
While both the membrane targets and the
centrosomes are made of proteins, the lo-
cation and form of these structures is not
wholly determined by the proteins that form
them. Indeed, centrosome structure and
membrane patterns as a whole convey
three-dimensional structural information
that helps determine the structure of the cy-
toskeleton and the location of its subunits
(McNiven & Porter 1992:313-329). More-
over, the centrioles that compose the cen-
trosomes replicate independently of DNA
replication (Lange et al. 2000:235-249,
Marshall & Rosenbaum 2000:187-205).
The daughter centriole receives its form
from the overall structure of the mother
centriole, not from the individual gene
products that constitute it (Lange et al.
2000). In ciliates, microsurgery on cell
membranes can produce heritable changes
in membrane patterns, even though the
DNA of the ciliates has not been altered
(Sonneborn 1970:1-13, Frankel 1980:607-
623; Nanney 1983:163-170). This suggests
that membrane patterns (as opposed to
membrane constituents) are impressed di-
rectly on daughter cells. In both cases, form
is transmitted from parent three-dimension-
al structures to daughter three-dimensional
structures directly and is not wholly con-
tained in constituent proteins or genetic in-
formation (Moss 2004).

Thus, in each new generation, the form
and structure of the cell arises as the result
of both gene products and pre-existing
three-dimensional structure and organiza-
tion. Cellular structures are built from pro-
teins, but proteins find their way to correct
locations in part because of pre-existing
three-dimensional patterns and organization
inherent in cellular structures. Pre-existing
three-dimensional form present in the pre-

ceding generation (whether inherent in the
cell membrane, the centrosomes, the cyto-
skeleton or other features of the fertilized
egg) contributes to the production of form
in the next generation. Neither structural
proteins alone, nor the genes that code for
them, are sufficient to determine the three-
dimensional shape and structure of the en-
tities they form. Gene products provide nec-
essary, but not sufficient conditions, for the
development of three-dimensional structure
within cells, organs and body plans (Harold
1995:2767). But if this is so, then natural
selection acting on genetic variation alone
cannot produce the new forms that arise in
history of life.

Self-Organizational Models

Of course, neo-Darwinism is not the only
evolutionary theory for explaining the ori-
gin of novel biological form. Kauffman
(1995) doubts the efficacy of the mutation/
selection mechanism. Nevertheless, he has
advanced a self-organizational theory to ac-
count for the emergence of new form, and
presumably the information necessary to
generate it. Whereas neo-Darwinism at-
tempts to explain new form as the conse-
quence of selection acting on random mu-
tation, Kauffman suggests that selection
acts, not mainly on random variations, but
on emergent patterns of order that self-
organize via the laws of nature.

Kauffman (1995:47-92) illustrates how
this might work with various model sys-
tems in a computer environment. In one, he
conceives a system of buttons connected by
strings. Buttons represent novel genes or
gene products; strings represent the law-like
forces of interaction that obtain between
gene products — i.e., proteins. Kauffman
suggests that when the complexity of the
system (as represented by the number of
buttons and strings) reaches a critical
threshold, new modes of organization can
arise in the system “for free” — that is, nat-
urally and spontaneously — after the manner
of a phase transition in chemistry.

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PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON

Another model that Kauffman develops
is a system of interconnected lights. Each
light can flash in a variety of states— on,
off, twinkling, etc. Since there is more than
one possible state for each light, and many
lights, there are a vast number of possible
states that the system can adopt. Further, in
his system, rules determine how past states
will influence future states. Kauffman as-
serts that, as a result of these rules, the sys-
tem will, if properly tuned, eventually pro-
duce a kind of order in which a few basic
patterns of light activity recur with greater-
than-random frequency. Since these actual
patterns of light activity represent a small
portion of the total number of possible
states in which the system can reside, Kauf-
man seems to imply that self-organizational
laws might similarly result in highly im-
probable biological outcomes— perhaps
even sequences (of bases or amino acids)
within a much larger sequence space of
possibilities.

Do these simulations of self-organiza-
tional processes accurately model the origin
of novel genetic information? It is hard to
think so.

First, in both examples, Kaufmann pre-
supposes but does not explain significant
sources of preexisting information. In his
buttons-and-strings system, the buttons rep-
resent proteins, themselves packets of CSI,
and the result of pre-existing genetic infor-
mation. Where does this information come
from? Kauffman (1995) doesn’t say, but the
origin of such information is an essential
part of what needs to be explained in the
history of life. Similarly, in his light sys-
tem, the order that allegedly arises for “for
free” actually arises only if the programmer
of the model system “tunes” it in such a
way as to keep it from either (a) generating
an excessively rigid order or (b) devolving
into chaos (pp. 86-88). Yet this necessary
tuning involves an intelligent programmer
selecting certain parameters and excluding
others — that is, inputting information.

Second, Kauffman’s model systems are
not constrained by functional consider-

ations and thus are not analogous to biolog-
ical systems. A system of interconnected
lights governed by pre-programmed rules
may well settle into a small number of pat-
terns within a much larger space of possi-
bilities. But because these patterns have no
function, and need not meet any functional
requirements, they have no specificity anal-
ogous to that present in actual organisms.
Instead, examination of Kauffman’s (1995)
model systems shows that they do not pro-
duce sequences or systems characterized by
specified complexity, but instead by large
amounts of symmetrical order or internal
redundancy interspersed with aperiodicity
or (mere) complexity (pp. 53, 89, 102). Get-
ting a law-governed system to generate re-
petitive patterns of flashing lights, even
with a certain amount of variation, is clearly
interesting, but not biologically relevant.
On the other hand, a system of lights flash-
ing the title of a Broadway play would
model a biologically relevant self-organi-
zational process, at least if such a meaning-
ful or functionally specified sequence arose
without intelligent agents previously pro-
gramming the system with equivalent
amounts of CSI. In any case, Kauffman’s
systems do not produce specified complex-
ity, and thus do not offer promising models
for explaining the new genes and proteins
that arose in the Cambrian.

Even so, Kauffman suggests that his self-
organizational models can specifically elu-
cidate aspects of the Cambrian explosion.
According to Kauffman (1995:199-201),
new Cambrian animals emerged as the re-
sult of “long jump” mutations that estab-
lished new body plans in a discrete rather
than gradual fashion. He also recognizes
that mutations affecting early development
are almost inevitably harmful. Thus, he
concludes that body plans, once established,
will not change, and that any subsequent
evolution must occur within an established
body plan (Kauffman 1995:201). And in-
deed, the fossil record does show a curious
(from a neo-Darwinian point of view) top-
down pattern of appearance, in which high-

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er taxa (and the body plans they represent)
appear first, only later to be followed by the
multiplication of lower taxa representing
variations within those original body de-
signs (Erwin et al. 1987, Lewin 1988, Val-
entine & Jablonski 2003:518). Further, as
Kauffman expects, body plans appear sud-
denly and persist without significant modi-
fication over time.

But here, again, Kauffman begs the most
important question, which is: what produc-
es the new Cambrian body plans in the first
place? Granted, he invokes “long jump mu-
tations” to explain this, but he identifies no
specific self-organizational process that can
produce such mutations. Moreover, he con-
cedes a principle that undermines the plau-
sibility of his own proposal. Kauffman ac-
knowledges that mutations that occur early
in development are almost inevitably dele-
terious. Yet developmental biologists know
that these are the only kind of mutations
that have a realistic chance of producing
large-scale evolutionary change — i.e., the
big jumps that Kauffman invokes. Though
Kauffman repudiates the neo-Darwinian re-
liance upon random mutations in favor of
self-organizing order, in the end, he must
invoke the most implausible kind of ran-
dom mutation in order to provide a self-
organizational account of the new Cambri-
an body plans. Clearly, his model is not suf-
ficient.

Punctuated Equilibrium

Of course, still other causal explanations
have been proposed. During the 1970s, the
paleontologists Eldredge and Gould (1972)
proposed the theory of evolution by punc-
tuated equilibrium in order to account for a
pervasive pattern of “sudden appearance”
and “stasis” in the fossil record. Though
advocates of punctuated equilibrium were
mainly seeking to describe the fossil record
more accurately than earlier gradualist neo-
Darwinian models had done, they did also
propose a mechanism — known as species
selection — by which the large morphologi-

cal jumps evident in fossil record might
have been produced. According to punctua-
tionalists, natural selection functions more
as a mechanism for selecting the fittest spe-
cies rather than the most-fit individual
among a species. Accordingly, on this mod-
el, morphological change should occur in
larger, more discrete intervals than it would
given a traditional neo-Darwinian under-
standing.

Despite its virtues as a descriptive model
of the history of life, punctuated equilibri-
um has been widely criticized for failing to
provide a mechanism sufficient to produce
the novel form characteristic of higher tax-
onomic groups. For one thing, critics have
noted that the proposed mechanism of
punctuated evolutionary change simply
lacked the raw material upon which to
work. As Valentine and Erwin (1987) note,
the fossil record fails to document a large
pool of species prior to the Cambrian. Yet
the proposed mechanism of species selec-
tion requires just such a pool of species
upon which to act. Thus, they conclude that
the mechanism of species selection proba-
bly does not resolve the problem of the or-
igin of the higher taxonomic groups (p.
96). 8 Further, punctuated equilibrium has
not addressed the more specific and fun-
damental problem of explaining the origin
of the new biological information (whether
genetic or epigenetic) necessary to produce
novel biological form. Advocates of punc-
tuated equilibrium might assume that the
new species (upon which natural selection
acts) arise by known micro-evolutionary
processes of speciation (such as founder ef-

8 Erwin (2004:21), although friendly to the possibil-
ity of species selection, argues that Gould provides lit-
tle evidence for its existence. “The difficulty” writes
Erwin of species selection, “. . . is that we must rely
on Gould’s arguments for theoretical plausibility and
sufficient relative frequency. Rarely is a mass of data
presented to justify and support Gould’s conclusion.”
Indeed, Gould (2002) himself admitted that species se-
lection remains largely a hypothetical construct: “I
freely admit that well-documented cases of species se-
lection do not permeate the literature” (p. 710).

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feet, genetic drift or bottleneck effect) that
do not necessarily depend upon mutations
to produce adaptive changes. But, in that
case, the theory lacks an account of how
the specifically higher taxa arise. Species
selection will only produce more fit species.
On the other hand, if punctuationalists as-
sume that processes of genetic mutation can
produce more fundamental morphological
changes and variations, then their model be-
comes subject to the same problems as neo-
Darwinism (see above). This dilemma is
evident in Gould (2002:710) insofar as his
attempts to explain adaptive complexity in-
evitably employ classical neo-Darwinian
modes of explanation. 9

Structuralism

Another attempt to explain the origin of
form has been proposed by the structuralists
such as Gerry Webster and Brian Goodwin
(1984, 1996). These biologists, drawing on
the earlier work of D’Arcy Thompson
(1942), view biological form as the result
of structural constraints imposed upon mat-
ter by morphogenetic rules or laws. For rea-
sons similar to those discussed above, the
structuralists have insisted that these gen-
erative or morphogenetic rules do not reside
in the lower level building materials of or-

9 “I do not deny either the wonder, or the powerful
importance, of organized adaptive complexity. I rec-
ognize that we know no mechanism for the origin of
such organismal features other than conventional nat-
ural selection at the organismic level — for the sheer
intricacy and elaboration of good biomechanical de-
sign surely precludes either random production, or in-
cidental origin as a side consequence of active pro-
cesses at other levels” (Gould 2002:710). “Thus, we
do not challenge the efficacy or the cardinal impor-
tance of organismal selection. As previously discussed,
I fully agree with Dawkins (1986) and others that one
cannot invoke a higher-level force like species selec-
tion to explain ‘things that organisms do’ — in partic-
ular, the stunning panoply of organismic adaptations
that has always motivated our sense of wonder about
the natural world, and that Darwin (1859) described,
in one of his most famous lines (3), as ‘that perfection
of structure and coadaptation which most justly excites
our admiration’ ” (Gould 2002:886).

ganisms, whether in genes or proteins.
Webster and Goodwin (1984:510-511) fur-
ther envision morphogenetic rules or laws
operating ahistorically, similar to the way
in which gravitational or electro-magnetic
laws operate. For this reason, structuralists
see phylogeny as of secondary importance
in understanding the origin of the higher
taxa, though they think that transformations
of form can occur. For structuralists, con-
straints on the arrangement of matter arise
not mainly as the result of historical contin-
gencies — such as environmental changes or
genetic mutations — but instead because of
the continuous ahistorical operation of fun-
damental laws of form — laws that organize
or inform matter.

While this approach avoids many of the
difficulties currently afflicting neo-Darwin-
ism (in particular those associated with its
“genocentricity”), critics (such as Maynard
Smith 1986) of structuralism have argued
that the structuralist explanation of form
lacks specificity. They note that structural-
ists have been unable to say just where laws
of form reside — whether in the universe, or
in every possible world, or in organisms as
a whole, or in just some part of organisms.
Further, according to structuralists, morpho-
genetic laws are mathematical in character.
Yet, structuralists have yet to specify the
mathematical formulae that determine bio-
logical forms.

Others (Yockey 1992; Polanyi 1967,
1968; Meyer 2003) have questioned wheth-
er physical laws could in principle generate
the kind of complexity that characterizes bi-
ological systems. Structuralists envision the
existence of biological laws that produce
form in much the same way that physical
laws produce form. Yet the forms that phys-
icists regard as manifestations of underlying
laws are characterized by large amounts of
symmetric or redundant order, by relatively
simple patterns such as vortices or gravi-
tational fields or magnetic lines of force. In-
deed, physical laws are typically expressed
as differential equations (or algorithms) that
almost by definition describe recurring phe-

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229

nomena — patterns of compressible “order”
not “complexity” as defined by algorithmic
information theory (Yockey 1992:77-83).
Biological forms, by contrast, manifest
greater complexity and derive in ontogeny
from highly complex initial conditions —
i.e., non-redundant sequences of nucleotide
bases in the genome and other forms of in-
formation expressed in the complex and ir-
regular three-dimensional topography of the
organism or the fertilized egg. Thus, the
kind of form that physical laws produce is
not analogous to biological form — at least
not when compared from the standpoint of
(algorithmic) complexity. Further, physical
laws lack the information content to specify
biology systems. As Polanyi (1967, 1968)
and Yockey (1992:290) have shown, the
laws of physics and chemistry allow, but do
not determine, distinctively biological
modes of organization. In other words, liv-
ing systems are consistent with, but not de-
ducible, from physical-chemical laws
(1992:290).

Of course, biological systems do manifest
some reoccurring patterns, processes and be-
haviors. The same type of organism devel-
ops repeatedly from similar ontogenetic pro-
cesses in the same species. Similar processes
of cell division re-occur in many organisms.
Thus, one might describe certain biological
processes as law-governed. Even so, the ex-
istence of such biological regularities does
not solve the problem of the origin of form
and information, since the recurring process-
es described by such biological laws (if there
be such laws) only occur as the result of pre-
existing stores of (genetic and/or epigenetic)
information and these information-rich ini-
tial conditions impose the constraints that
produce the recurring behavior in biological
systems. (For example, processes of cell di-
vision recur with great frequency in organ-
isms, but depend upon information-rich
DNA and proteins molecules.) In other
words, distinctively biological regularities
depend upon pre-existing biological infor-
mation. Thus, appeals to higher-level biolog-
ical laws presuppose, but do not explain, the

origination of the information necessary to
morphogenesis.

Thus, structuralism faces a difficult in
principle dilemma. On the one hand, phys-
ical laws produce very simple redundant
patterns that lack the complexity character-
istic of biological systems. On the other
hand, distinctively biological laws — if there
are such laws — depend upon pre-existing
information-rich structures. In either case,
laws are not good candidates for explaining
the origination of biological form or the in-
formation necessary to produce it.

Cladism: An Artifact of Classification?

Some cladists have advanced another ap-
proach to the problem of the origin of form,
specifically as it arises in the Cambrian.
They have argued that the problem of the
origin of the phyla is an artifact of the clas-
sification system, and therefore, does not
require explanation. Budd and Jensen
(2000), for example, argue that the problem
of the Cambrian explosion resolves itself if
one keeps in mind the cladistic distinction
between “stem” and “crown” groups.
Since crown groups arise whenever new
characters are added to simpler more an-
cestral stem groups during the evolutionary
process, new phyla will inevitably arise
once a new stem group has arisen. Thus,
for Budd and Jensen what requires expla-
nation is not the crown groups correspond-
ing to the new Cambrian phyla, but the ear-
lier more primitive stem groups that pre-
sumably arose deep in the Proterozoic. Yet
since these earlier stem groups are by def-
inition less derived, explaining them will be
considerably easier than explaining the or-
igin of the Cambrian animals de novo. In
any case, for Budd and Jensen the explo-
sion of new phyla in the Cambrian does not
require explanation. As they put it, “given
that the early branching points of major
clades is an inevitable result of clade di-
versification, the alleged phenomenon of
the phyla appearing early and remaining
morphologically static is not seen to require

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PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON

particular explanation” (Budd & Jensen
2000:253).

While superficially plausible, perhaps,
Budd and Jensen’s attempt to explain away
the Cambrian explosion begs crucial ques-
tions. Granted, as new characters are added
to existing forms, novel morphology and
greater morphological disparity will likely
result. But what causes new characters to
arise? And how does the information nec-
essary to produce new characters originate?
Budd and Jensen do not specify. Nor can
they say how derived the ancestral forms
are likely to have been, and what processes,
might have been sufficient to produce them.
Instead, they simply assume the sufficiency
of known neo-Darwinian mechanisms
(Budd & Jensen 2000:288). Yet, as shown
above, this assumption is now problematic.
In any case, Budd and Jensen do not ex-
plain what causes the origination of biolog-
ical form and information.

Convergence and Teleological Evolution

More recently, Conway Morris (2000,
2003c) has suggested another possible ex-
planation based on the tendency for evolu-
tion to converge on the same structural
forms during the history of life. Conway
Morris cites numerous examples of organ-
isms that possess very similar forms and
structures, even though such structures are
often built from different material sub-
strates and arise (in ontogeny) by the ex-
pression of very different genes. Given the
extreme improbability of the same struc-
tures arising by random mutation and se-
lection in disparate phytogenies, Conway
Morris argues that the pervasiveness of
convergent structures suggests that evolu-
tion may be in some way “channeled” to-
ward similar functional and/or structural
endpoints. Such an end-directed under-
standing of evolution, he admits, raises the
controversial prospect of a teleological or
purposive element in the history of life. For
this reason, he argues that the phenomenon
of convergence has received less attention

than it might have otherwise. Nevertheless,
he argues that just as physicists have re-
opened the question of design in their dis-
cussions of anthropic fine-tuning, the ubiq-
uity of convergent structures in the history
of life has led some biologists (Denton
1998) to consider extending teleological
thinking to biology. And, indeed, Conway
Morris himself intimates that the evolution-
ary process might be “underpinned by a
purpose” (2000:8, 2003b:511).

Conway Morris, of course, considers this
possibility in relation to a very specific as-
pect of the problem of organismal form,
namely, the problem of explaining why the
same forms arise repeatedly in so many dis-
parate lines of decent. But this raises a
question. Could a similar approach shed ex-
planatory light on the more general causal
question that has been addressed in this re-
view? Could the notion of purposive design
help provide a more adequate explanation
for the origin of organismal form generally?
Are there reasons to consider design as an
explanation for the origin of the biological
information necessary to produce the higher
taxa and their corresponding morphological
novelty?

The remainder of this review will suggest
that there are such reasons. In so doing, it
may also help explain why the issue of tel-
eology or design has re-emerged within the
scientific discussion of biological origins
(Denton 1986, 1998; Thaxton et al. 1992;
Kenyon & Mills 1996; Behe 1996, 2004;
Dembski 1998, 2002, 2004; Conway Mor-
ris 2000, 2003a, 2003b; Lonnig 2001; Lon-
nig & Saedler 2002; Nelson & Wells 2003;
Meyer 2003, 2004; Bradley 2004) and why
some scientists and philosophers of science
have considered teleological explanations
for the origin of form and information de-
spite strong methodological prohibitions
against design as a scientific hypothesis
(Gillespie 1979, Lenior 1982:4).

First, the possibility of design as an ex-
planation follows logically from a consid-
eration of the deficiencies of neo-Darwin-
ism and other current theories as explana-

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231

tions for some of the more striking “ap-
pearances of design” in biological systems.
Neo-Darwinists such as Ayala (1994:5),
Dawkins (1986:1), Mayr (1982:xi-xii) and
Lewontin (1978) have long acknowledged
that organisms appear to have been de-
signed. Of course, neo-Darwinists assert
that what Ayala (1994:5) calls the “obvious
design” of living things is only apparent
since the selection/mutation mechanism can
explain the origin of complex form and or-
ganization in living systems without an ap-
peal to a designing agent. Indeed, neo-Dar-
winists affirm that mutation and selection —
and perhaps other similarly undirected
mechanisms — are fully sufficient to explain
the appearance of design in biology. Self-
organizational theorists and punctuational-
ists modify this claim, but affirm its essen-
tial tenet. Self-organization theorists argue
that natural selection acting on self-organiz-
ing order can explain the complexity of liv-
ing things — again, without any appeal to
design. Punctuationalists similarly envision
natural selection acting on newly arising
species with no actual design involved.

And clearly, the neo-Darwinian mecha-
nism does explain many appearances of de-
sign, such as the adaptation of organisms to
specialized environments that attracted the
interest of 19th century biologists. More
specifically, known micro-evolutionary pro-
cesses appear quite sufficient to account for
changes in the size of Galapagos finch
beaks that have occurred in response to var-
iations in annual rainfall and available food
supplies (Weiner 1994, Grant 1999).

But does neo-Darwinism, or any other
fully materialistic model, explain all ap-
pearances of design in biology, including
the body plans and information that char-
acterize living systems? Arguably, biologi-
cal forms — such as the structure of a cham-
bered nautilus, the organization of a trilo-
bite, the functional integration of parts in
an eye or molecular machine — attract our
attention in part because the organized
complexity of such systems seems reminis-
cent of our own designs. Yet, this review

has argued that neo-Darwinism does not
adequately account for the origin of all ap-
pearances of design, especially if one con-
siders animal body plans, and the informa-
tion necessary to construct them, as espe-
cially striking examples of the appearance
of design in living systems. Indeed, Dawk-
ins (1995:11) and Gates (1996:228) have
noted that genetic information bears an un-
canny resemblance to computer software or
machine code. For this reason, the presence
of CSI in living organisms, and the discon-
tinuous increases of CSI that occurred dur-
ing events such as the Cambrian explosion,
appears at least suggestive of design.

Does neo-Darwinism or any other purely
materialistic model of morphogenesis ac-
count for the origin of the genetic and other
forms of CSI necessary to produce novel
organismal form? If not, as this review has
argued, could the emergence of novel in-
formation-rich genes, proteins, cell types
and body plans have resulted from actual
design, rather than a purposeless process
that merely mimics the powers of a design-
ing intelligence? The logic of neo-Darwin-
ism, with its specific claim to have account-
ed for the appearance of design, would it-
self seem to open the door to this possibil-
ity. Indeed, the historical formulation of
Darwinism in dialectical opposition to the
design hypothesis (Gillespie 1979), coupled
with neo-Darwinism’s inability to account
for many salient appearances of design in-
cluding the emergence of form and infor-
mation, would seem logically to re-open the
possibility of actual (as opposed to appar-
ent) design in the history of life.

A second reason for considering design
as an explanation for these phenomena fol-
lows from the importance of explanatory
power to scientific theory evaluation and
from a consideration of the potential ex-
planatory power of the design hypothesis.
Studies in the methodology and philosophy
of science have shown that many scientific
theories, particularly in the historical sci-
ences, are formulated and justified as infer-
ences to the best explanation (Lipton 1991:

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PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON

32-88, Brush 1989:1124-1129, Sober
2000:44). Historical scientists, in particular,
assess or test competing hypotheses by
evaluating which hypothesis would, if true,
provide the best explanation for some set of
relevant data (Meyer 1991, 2002; Cleland
2001:987-989, 2002:474-496). 10 Those

10 Theories in the historical sciences typically make
claims about what happened in the past, or what hap-
pened in the past to cause particular events to occur
(Meyer 1991:57-72). For this reason, historical sci-
entific theories are rarely tested by making predictions
about what will occur under controlled laboratory con-
ditions (Cleland 2001:987, 2002:474-496). Instead,
such theories are usually tested by comparing their ex-
planatory power against that of their competitors with
respect to already known facts. Even in the case in
which historical theories make claims about past caus-
es they usually do so on the basis of pre-existing
knowledge of cause and effect relationships. Neverthe-
less, prediction may play a limited role in testing his-
torical scientific theories since such theories may have
implications as to what kind of evidence is likely to
emerge in the future. For example, neo-Darwinism af-
firms that new functional sections of the genome arise
by trial and error process of mutation and subsequent
selection. For this reason, historically many neo-Dar-
winists expected or predicted that the large non-coding
regions of the genome — so-called “junk DNA — would
lack function altogether (Orgel & Crick 1 980). On this
line of thinking, the non-functional sections of the ge-
nome represent nature’s failed experiments that remain
in the genome as a kind of artifact of the past activity
of the mutation and selection process. Advocates of
the design hypotheses on the other hand, would have
predicted that non-coding regions of the genome might
well reveal hidden functions, not only because design
theorists do not think that new genetic information
arises by a trial and error process of mutation and se-
lection, but also because designed systems are often
functionally polyvalent. Even so, as new studies reveal
more about the functions performed by the non-coding
regions of the genome (Gibbs 2003), the design hy-
pothesis can no longer be said to make this claim in
the form of a specifically future-oriented prediction.
Instead, the design hypothesis might be said to gain
confirmation or support from its ability to explain this
now known evidence, albeit after the fact. Of course,
neo-Darwinists might also amend their original pre-
diction using various auxiliary hypotheses to explain
away the presence of newly discovered functions in
the non-coding regions of DNA. In both cases, consid-
erations of ex post facto explanatory power re-emerge
as central to assessing and testing competing historical
theories.

with greater explanatory power are typical-
ly judged to be better, more probably true,
theories. Darwin (1896:437) used this
method of reasoning in defending his the-
ory of universal common descent. More-
over, contemporary studies on the method
of “inference to the best explanation” have
shown that determining which among a set
of competing possible explanations consti-
tutes the best depends upon judgments
about the causal adequacy, or “causal pow-
ers,” of competing explanatory entities
(Lipton 1991:32-88). In the historical sci-
ences, uniformitarian and/or actualistic
(Gould 1965, Simpson 1970, Rutten 1971,
Hooykaas 1975) canons of method suggest
that judgments about causal adequacy
should derive from our present knowledge
of cause and effect relationships. For his-
torical scientists, “the present is the key to
the past” means that present experience-
based knowledge of cause and effect rela-
tionships typically guides the assessment of
the plausibility of proposed causes of past
events.

Yet it is precisely for this reason that cur-
rent advocates of the design hypothesis
want to reconsider design as an explanation
for the origin of biological form and infor-
mation. This review, and much of the lit-
erature it has surveyed, suggests that four
of the most prominent models for explain-
ing the origin of biological form fail to pro-
vide adequate causal explanations for the
discontinuous increases of CSI that are re-
quired to produce novel morphologies. Yet,
we have repeated experience of rational and
conscious agents — in particular ourselves —
generating or causing increases in complex
specified information, both in the form of
sequence-specific lines of code and in the
form of hierarchically arranged systems of
parts.

In the first place, intelligent human
agents — in virtue of their rationality and
consciousness — have demonstrated the
power to produce information in the form
of linear sequence-specific arrangements of
characters. Indeed, experience affirms that

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233

information of this type routinely arises
from the activity of intelligent agents. A
computer user who traces the information
on a screen back to its source invariably
comes to a mind — that of a software engi-
neer or programmer. The information in a
book or inscription ultimately derives from
a writer or scribe — from a mental, rather
than a strictly material, cause. Our experi-
ence-based knowledge of information-flow
confirms that systems with large amounts of
specified complexity (especially codes and
languages) invariably originate from an in-
telligent source — from a mind or personal
agent. As Quastler (1964) put it, the “cre-
ation of new information is habitually as-
sociated with conscious activity” (p. 16).
Experience teaches this obvious truth.

Further, the highly specified hierarchical
arrangements of parts in animal body plans
also suggest design, again because of our
experience of the kinds of features and sys-
tems that designers can and do produce. At
every level of the biological hierarchy, or-
ganisms require specified and highly im-
probable arrangements of lower-level con-
stituents in order to maintain their form and
function. Genes require specified arrange-
ments of nucleotide bases; proteins require
specified arrangements of amino acids; new
cell types require specified arrangements of
systems of proteins; body plans require spe-
cialized arrangements of cell types and or-
gans. Organisms not only contain informa-
tion-rich components (such as proteins and
genes), but they comprise information-rich
arrangements of those components and the
systems that comprise them. Yet we know,
based on our present experience of cause
and effect relationships, that design engi-
neers — possessing purposive intelligence
and rationality — have the ability to produce
information-rich hierarchies in which both
individual modules and the arrangements of
those modules exhibit complexity and spec-
ificity — information so defined. Individual
transistors, resistors, and capacitors exhibit
considerable complexity and specificity of
design; at a higher level of organization.

their specific arrangement within an inte-
grated circuit represents additional infor-
mation and reflects further design. Con-
scious and rational agents have, as part of
their powers of purposive intelligence, the
capacity to design information-rich parts
and to organize those parts into functional
information-rich systems and hierarchies.
Further, we know of no other causal entity
or process that has this capacity. Clearly,
we have good reason to doubt that mutation
and selection, self-organizational processes
or laws of nature, can produce the infor-
mation-rich components, systems, and body
plans necessary to explain the origination
of morphological novelty such as that
which arises in the Cambrian period.

There is a third reason to consider pur-
pose or design as an explanation for the or-
igin of biological form and information:
purposive agents have just those necessary
powers that natural selection lacks as a con-
dition of its causal adequacy. At several
points in the previous analysis, we saw that
natural selection lacked the ability to gen-
erate novel information precisely because it
can only act after new functional CSI has
arisen. Natural selection can favor new pro-
teins, and genes, but only after they per-
form some function. The job of generating
new functional genes, proteins and systems
of proteins therefore falls entirely to ran-
dom mutations. Yet without functional cri-
teria to guide a search through the space of
possible sequences, random variation is
probabilistically doomed. What is needed is
not just a source of variation (i.e., the free-
dom to search a space of possibilities) or a
mode of selection that can operate after the
fact of a successful search, but instead a
means of selection that (a) operates during
a search — before success — and that (b) is
guided by information about, or knowledge
of, a functional target.

Demonstration of this requirement has
come from an unlikely quarter: genetic al-
gorithms. Genetic algorithms are programs
that allegedly simulate the creative power
of mutation and selection. Dawkins and

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PROCEEDINGS OF THE BIOLOGICAL SOCIETY OF WASHINGTON

Kuppers, for example, have developed
computer programs that putatively simulate
the production of genetic information by
mutation and natural selection (Dawkins
1986:47-49, Kuppers 1987:355-369). Nev-
ertheless, as shown elsewhere (Meyer 1998:
127-128, 2003:247-248), these programs
only succeed by the illicit expedient of pro-
viding the computer with a “target se-
quence” and then treating relatively greater
proximity to future function (i.e., the target
sequence), not actual present function, as a
selection criterion. As Berlinski (2000) has
argued, genetic algorithms need something
akin to a “forward looking memory” in or-
der to succeed. Yet such foresighted selec-
tion has no analogue in nature. In biology,
where differential survival depends upon
maintaining function, selection cannot oc-
cur before new functional sequences arise.
Natural selection lacks foresight.

What natural selection lacks, intelligent
selection — purposive or goal-directed de-
sign — provides. Rational agents can arrange
both matter and symbols with distant goals
in mind. In using language, the human
mind routinely “finds” or generates highly
improbable linguistic sequences to convey
an intended or preconceived idea. In the
process of thought, functional objectives
precede and constrain the selection of
words, sounds and symbols to generate
functional (and indeed meaningful) se-
quences from among a vast ensemble of
meaningless alternative combinations of
sound or symbol (Denton 1986:309-311).
Similarly, the construction of complex tech-
nological objects and products, such as
bridges, circuit boards, engines and soft-
ware, result from the application of goal-
directed constraints (Polanyi 1967, 1968).
Indeed, in all functionally integrated com-
plex systems where the cause is known by
experience or observation, design engineers
or other intelligent agents applied boundary
constraints to limit possibilities in order to
produce improbable forms, sequences or
structures. Rational agents have repeatedly
demonstrated the capacity to constrain the

possible to actualize improbable but initial-
ly unrealized future functions. Repeated ex-
perience affirms that intelligent agents
(minds) uniquely possess such causal pow-
ers.

Analysis of the problem of the origin of
biological information, therefore, exposes a
deficiency in the causal powers of natural
selection that corresponds precisely to pow-
ers that agents are uniquely known to pos-
sess. Intelligent agents have foresight. Such
agents can select functional goals before
they exist. They can devise or select mate-
rial means to accomplish those ends from
among an array of possibilities and then ac-
tualize those goals in accord with a pre con-
ceived design plan or set of functional re-
quirements. Rational agents can constrain
combinatorial space with distant outcomes
in mind. The causal powers that natural se-
lection lacks — almost by definition — are as-
sociated with the attributes of conscious-
ness and rationality — with purposive intel-
ligence. Thus, by invoking design to ex-
plain the origin of new biological
information, contemporary design theorists
are not positing an arbitrary explanatory el-
ement unmotivated by a consideration of
the evidence. Instead, they are positing an
entity possessing precisely the attributes
and causal powers that the phenomenon in
question requires as a condition of its pro-
duction and explanation.

Conclusion

An experience-based analysis of the
causal powers of various explanatory hy-
potheses suggests purposive or intelligent
design as a causally adequate — and perhaps
the most causally adequate — explanation
for the origin of the complex specified in-
formation required to build the Cambrian
animals and the novel forms they represent.
For this reason, recent scientific interest in
the design hypothesis is unlikely to abate as
biologists continue to wrestle with the prob-
lem of the origination of biological form
and the higher taxa.

VOLUME 1 17, NUMBER 2

235

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